[赖氨酸（K）乙酰转移酶2A通过经典Wnt信号通路影响牙周膜干细胞的成骨分化]
[K (lysine) acetyltransferase 2A affects the osteogenic differentiation of periodontal ligament stem cells through the canonical Wnt pathway].
作者信息
Wucheng Guo, Jieli Cheng, Zhengyi Yang, Yi Zhang, Enliang He, Jun Qian, Jingjing Song, Jin Sun, Lin Yuan
机构信息
Dept. of Stomatology, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou 510120, China.
Stomatological Disease Center, Shenzhen Maternal and Child Health Care Hospital, Southern Medical University, Shenzhen 518048, China.
出版信息
Hua Xi Kou Qiang Yi Xue Za Zhi. 2018 Feb 1;36(1):39-45. doi: 10.7518/hxkq.2018.01.008.
OBJECTIVE
This study aims to investigate the mechanism of K (lysine) acetyltransferase 2A (KAT2A) regulation and control on the osteogenic differentiation of periodontal ligament stem cells (PDLSCs).
METHODS
The expression levels of KAT2A in PDLSCs were compared from each generation of the normal (H-PDLSCs) and periodontitis tissues (P-PDLSCs). The influences of KAT2A gene interference on the osteogenic differentiation of PDLSCs were also detected. In addition, the influences of the KAT2A gene interference to the canonical Wnt pathway and ligands were detected. The upstream and down-stream relationships between KAT2A and canonical Wnt pathway were also determined.
RESULTS
The decreased expression of KAT2A in PDLSCs from the inflammatory tissue in each generation was compared with that in PDLSCs from the healthy tissue, and the difference was statistically significant (P<0.05). When the KAT2A gene was disrupted, the osteogenesis ability of PDLSC was declined, and the difference was statistically significant (P<0.05). The canonical Wnt pathway was activated, and the antagonist Dickkopf-1 (DKK-1) was reduced. After the DKK-1 addition, the osteogenic differentiation of the disturbed PDLSCs was recovered, and KAT2A was unaffected.
CONCLUSIONS
The KAT2A expression in PDLSCs was decreased because of perio-dontitis. The classical Wnt pathway was activated to inhibit the osteogenic differentiation of the cells.
目的
本研究旨在探讨赖氨酸乙酰转移酶2A（KAT2A）调控牙周膜干细胞（PDLSCs）成骨分化的机制。
方法
比较正常组织（H-PDLSCs）和牙周炎组织（P-PDLSCs）各代PDLSCs中KAT2A的表达水平。检测KAT2A基因干扰对PDLSCs成骨分化的影响。此外，检测KAT2A基因干扰对经典Wnt通路及配体的影响。确定KAT2A与经典Wnt通路之间的上下游关系。
结果
各代炎症组织中PDLSCs的KAT2A表达水平均低于健康组织中的PDLSCs，差异有统计学意义（P<0.05）。KAT2A基因被破坏时，PDLSC的成骨能力下降，差异有统计学意义（P<0.05）。经典Wnt通路被激活，拮抗剂Dickkopf-1（DKK-1）减少。添加DKK-1后，受干扰的PDLSCs的成骨分化得以恢复，而KAT2A不受影响。
结论
牙周炎导致PDLSCs中KAT2A表达降低。经典Wnt通路被激活，抑制了细胞的成骨分化。
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